monee Myalgic = muscle pain

Encephalo = brain

Myel = central nervous system

Itis = inflammation

myalgic encephalomyelitis / m_e


- c_f_s / chronic_fatigue_syndrome

- cfids / chronic fatigue immune dysfunction syndrome

- nds /
neuroendocrineimmune dysfuction syndrome

- pvfs /
post-viral immune dysfunction syndrome

- fn / florence nightingale disease


About Myalgic Encephalomyelitis and Fibromyalgia

"Classified by the World Health Organization as a disease of the nervous system. ME is the subject of research by the Centers for Disease Control in the US and top researchers around the world"

Fibromyalgia Syndrome
Fibro = joint

Myalgia = muscle pain

"...Classified by the World Health Organization as a disease of the musculoskeletal system. Thought by many researchers to be a condition the same as, or related to ME.

What causes ME/CFS and FM?

The cause has not yet been identified. On-going research suggest that an infectious agent (possibly a virus) or other triggers invade brain and muscle cells, causing the immune system in some people to become chronically overactive.

Who, When and How Long?

ME and FM can be contracted by anyone at any age. A small minority of people recover completely, some experience a series of relapses and remissions, while in others the symptoms may persist for many years. An early and accurate diagnosis with immediate and appropriate treatment measures greatly enhances the chances for recovery.

The type, severity, and frequency of symptoms of ME and FM vary from one individual to another and often from day to day..."


"...myalgic encephalomyelitis (M.E.), [is] a multi-system disease adversely affecting the heart, brain, neuroendocrine, immune, and circulatory systems...Many different viruses, bacteria, or toxins may be involved in the etiology of the disease in combination with genetic factors. Studying research-based subsets is the key to scientific progress in this area of investigation. In a number of publications, Dr. A. Melvin Ramsay outlined a definitional framework that described abnormal muscle metabolism, circulatory impairment, and cerebral involvement. There is, however, a more current, research-updated criteria compiled by the Canadian Consensus Panel for ME/CFS, which includes neuroendocrine, immune, and cardiocirculatory symptoms as well as abnormal muscle metabolism, circulatory impairment, and cerebral/neurological involvement...Unfortunately, in 1988, what was historically known both as myalgic encephalomyelitis and as the well-documented epidemic neuromyasthenia was renamed “Chronic Fatigue Syndrome” by employees at the Centers for Disease Control (CDC), who imposed the misleading “fatigue” term onto patients and researchers. In 1994, more damage was done when the CDC broadened the definition for CFS to include many diverse, unrelated diseases, for which “CFS” became an umbrella term. Currently, a government-appointed name-change workgroup has proposed a new umbrella term, Neuroendocrineimmune Dysfunction Syndrome (NDS), under which Ramsay, Canadian, and other selection criteria subsets would be placed.

Ramsay's preliminary observations and identification of the essential features were well grounded, but in the years since Ramsay published, there has been a great deal of research that has increased our understanding of this disease. For example, mounting research indicates that orthostatic intolerance, in some cases involving a virally induced dysfunction of the autonomic nervous system, low plasma and/or erythrocyte volume, or left-ventricular failure upon postural stress according to new research, should be added as a separate and important feature of M.E. that occurs when the degree of illness is moderate or severe. The Canadian Clinical Case Definition lists neurally mediated hypotension, postural orthostatic tachycardia syndrome, cardiac arrhythmia, and neuroendocrine immune manifestations. While it also lists fatigue as a symptom, a more accurate use of language would be to use “muscle weakness and pain” or “delayed muscle recovery after exercise” as opposed to the vague and inaccurate term “fatigue” for muscle problems. We urge researchers and patients to eliminate the label of fatigue and focus instead on a neuroendocrine immune, cardiocirculatory model. In addition to what the Canadian Consensus Panel described, some research has shown respiratory chain deficits and damage to the mitochondrial DNA, and, when the degree of illness is severe, acquired myopathic changes in some subsets.

M.E. generally begins in childhood or early adulthood with an acute infection (although slow onset is also possible) resulting in immune dysregulation, and there is some evidence that mitochondrial dysfunction plays a role in the ensuing pathophysiology of M.E. and of other neurological diseases. Infections and/or environmental toxins, alone or in combination with genetic factors, may play a role in the etiology of the disease. Although we still do not have a universally accepted final theory as to why the body reacts in this way, research points to a cascade of events involving an abnormal neuroendocrine immune, cardiocirculatory response with immune system dysregulation (inflammation, low CD8’s [Klimas], and autoimmunity); post-exertional hypercoagulation and/or abnormal erythrocyte morphology with chronic and/or progressive post-exertional tissue hypoxia-ischemia; dysautonomia and neuroendocrine involvement such as elevated epinephrine, abnormal neural orthostatic responses to epinephrine, and low plasma and/or erythrocyte volume; and cardiomyopathy. Viral cardiomyopathy, viral encephalitis, and virally induced dysfunction of the autonomic nervous system may all contribute to the multi-system picture in a prominent subset of this disease, according to hypotheses for which researchers have presented evidence.

Others have argued that the muscle and neuroendocrine dysfunction may follow from inadequate oxygen delivery to tissues, either from coagulopathy, blood viscosity, and deposits of fibrin; or blood with high values of red cells with altered margins – or both. When the capacity of cells to take up and release oxygen is impaired, the body shifts to anaerobic metabolism, wherein incomplete metabolism of glycogen leads to the formation of lactic acid, which further impairs oxygen delivery. Brain, nerves, heart, skeletal muscles, and endocrine glands have higher requirements for oxygen and nutrient substrates, require more energy, and react to deficiencies with more serious consequences.

The mitochondria and respiratory chain are adversely affected by tissue hypoxia-ischemia; they are also adversely affected by elevated nitric oxide, another common finding in the disease. Some infectious agents also adversely affect the mitochondria. Mitochondrial metabolism is the principle source of energy intermediates as well as of free radicals. Acquired mitochondrial defects could be responsible for the neuronal degeneration. Mitochondrial respiratory chain dysfunction has been reported in association with primary mitochondrial DNA abnormalities. But defects in oxidative phosphorylation and increased free radical production have also been observed in diseases that are not due to inherited mitochondrial abnormalities. In these cases, the mitochondrial failure is likely to be an epiphenomenon that precipitates a secondary cascade of events. As in other conditions in which the respiratory chain is compromised, M.E. is a multi-system disease affecting many organ systems of the body. The end result of the above-described cascade may be a crisis in the cells of the skeletal muscles, heart, brain, kidney, endocrine, and other systems. Accumulated damage to the mitochondrial DNA over many years could lead to similar problems as in inherited mitochondrial diseases.

In her recent paper (Jan 01), "The Late Effects of ME," the well-known English ME specialist Dr. Betty Dowsett wrote: ".....FINAL STAGE (1,2) After a variable interval, a multi-system syndrome may develop, involving permanent damage to skeletal or cardiac muscle and to other "end organs" such as the liver, pancreas, endocrine glands and lymphoid tissues, signifying the further development of a lengthy chronic, mainly neurological condition with evidence of metabolic dysfunction in the brain stem. Yet, stabilization, albeit at a low level, can still be achieved by appropriate management and support. The death rate of 10% occurs almost entirely from end-organ damage within this group (mainly from cardiac or pancreatic failure)."..."





Complied by Jodi Bassett, 2004
- a hummingbird's guide to me/cfids - *information on living with severe myalgic encephalomyelitis /cfids

anomalous may_12th 050512
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